Selenium and selenoproteins in adipose tissue physiology and obesity
Tin`kov A. A., Aysuvakova O. P., Filippini T., Zhou J. -., Lei X. G., Gatiatulina E. R., Michalke B., Skal`naya M. G., Vinceti M., Ashner M., Skal`ny'j A. V.
Biomolecules
Vol.10, Issue4, Num.658
Опубликовано: 2020
Тип ресурса: Обзор
Аннотация:
Selenium (Se) homeostasis is tightly related to carbohydrate and lipid metabolism, but its possible roles in obesity development and in adipocyte metabolism are unclear. The objective of the present study is to review the current data on Se status in obesity and to discuss the interference between Se and selenoprotein metabolism in adipocyte physiology and obesity pathogenesis. The overview and meta-analysis of the studies on blood Se and selenoprotein P (SELENOP) levels, as well as glutathione peroxidase (GPX) activity in obese subjects, have yielded heterogenous and even conflicting results. Laboratory studies demonstrate that Se may modulate preadipocyte proliferation and adipogenic differentiation, and also interfere with insulin signaling, and regulate lipolysis. Knockout models have demonstrated that the selenoprotein machinery, including endoplasmic reticulum-resident selenoproteins together with GPXs and thioredoxin reductases (TXNRDs), are tightly related to adipocyte developm
Ключевые слова:
Adipocyte; Adipogenesis; Obesity; Selenium; Selenoprotein
selenium; selenoprotein; selenoprotein P; thioredoxin reductase; abdominal obesity; adipocyte; adipogenesis; adipose tissue; antioxidant activity; apoptosis; bariatric surgery; bioaccumulation; body fat; body mass; caloric intake; caloric restriction; carbohydrate metabolism; cell proliferation; cell survival; cell viability; cytokine production; cytotoxicity; diet supplementation; down regulation; dyslipidemia; endoplasmic reticulum; endoplasmic reticulum stress; energy balance; energy metabolism; environmental exposure; enzyme activity; fat mass; food intake; gene expression; gene mutation; genome-wide association study; glucose metabolism; glucose transport; homeostasis model assessment; hyperglycemia; hyperleptinemia; hyperlipidemia; insulin sensitivity; insulin signaling; insulin treatment; lipid diet; lipid metabolism; lipid storage; lipolysis; mesenchymal stem cell; metabolic syndrome X; mitochondrial membrane potential; morphometry; myelination; nerve degeneration; nitrosylatio
Язык текста: Английский
ISSN: 2218-273X
Tin`kov A. A. Aleksej Alekseevich 1989-
Aysuvakova O. P. Ol`ga Pavlovna 1982-
Filippini T.
Zhou J. -. J.-C.
Lei X. G.
Gatiatulina E. R.
Michalke B.
Skal`naya M. G. Margarita Gennadievna 1968-
Vinceti M.
Ashner M. Mikhae`l` 1955-
Skal`ny'j A. V. Anatolij Viktorovich 1962-
Тиньков А. А. Алексей Алексеевич 1989-
Айсувакова О. П. Ольга Павловна 1982-
Филиппини Т.
Жоу Й. -. Й.-C.
Леи Х. Г.
Гатиатюлина Е. Р.
Мичалке Б.
Скальная М. Г. Маргарита Геннадиевна 1968-
Винcети М.
Ашнер М. Михаэль 1955-
Скальный А. В. Анатолий Викторович 1962-
Selenium and selenoproteins in adipose tissue physiology and obesity
Текст визуальный непосредственный
Biomolecules
Vol.10, Issue4 Num.658
2020
Обзор
Adipocyte Adipogenesis Obesity Selenium Selenoprotein
selenium selenoprotein selenoprotein P thioredoxin reductase abdominal obesity adipocyte adipogenesis adipose tissue antioxidant activity apoptosis bariatric surgery bioaccumulation body fat body mass caloric intake caloric restriction carbohydrate metabolism cell proliferation cell survival cell viability cytokine production cytotoxicity diet supplementation down regulation dyslipidemia endoplasmic reticulum endoplasmic reticulum stress energy balance energy metabolism environmental exposure enzyme activity fat mass food intake gene expression gene mutation genome-wide association study glucose metabolism glucose transport homeostasis model assessment hyperglycemia hyperleptinemia hyperlipidemia insulin sensitivity insulin signaling insulin treatment lipid diet lipid metabolism lipid storage lipolysis mesenchymal stem cell metabolic syndrome X mitochondrial membrane potential morphometry myelination nerve degeneration nitrosylatio
Selenium (Se) homeostasis is tightly related to carbohydrate and lipid metabolism, but its possible roles in obesity development and in adipocyte metabolism are unclear. The objective of the present study is to review the current data on Se status in obesity and to discuss the interference between Se and selenoprotein metabolism in adipocyte physiology and obesity pathogenesis. The overview and meta-analysis of the studies on blood Se and selenoprotein P (SELENOP) levels, as well as glutathione peroxidase (GPX) activity in obese subjects, have yielded heterogenous and even conflicting results. Laboratory studies demonstrate that Se may modulate preadipocyte proliferation and adipogenic differentiation, and also interfere with insulin signaling, and regulate lipolysis. Knockout models have demonstrated that the selenoprotein machinery, including endoplasmic reticulum-resident selenoproteins together with GPXs and thioredoxin reductases (TXNRDs), are tightly related to adipocyte developm